Ischemic acute renal failure created by infusing norepinephrine (NE) into one or both renal arteries results in a severe, sustained (up to 24 hours) decrease in glomerular filtration rate (GFR). Both mannitol and furosemide have been demonstrated to be protective in this model, in that their administration for 30 minutes prior to NE infusion results in a measureable recovery of GFR by 3 hours post - NE. Isotonic saline, however, does not alleviate the decrease in GFR. Currently, other agents are being used to further solidify our feeling that early increases in solute excretion effected by the presence of non-reabsorbable solutes (mannitol and in the case of furosemide, saline) cause intratubular pressure to rise. This increase in the intratubular pressure helps to dislodge the debris which might accumulate in the nephron following the ischemic insult. This debris could cause 1) a sufficient degree of obstruction such that urine flow would be minimal and 2) a reduction in effective filtration pressure such that GFR would be reduced. The agents currently being studied by a combination of clearance and micropuncture studies are hypertonic saline, polyethylene glycol and verapamil.